CD48 is a GPI-anchored protein that exists in both membrane-bound and soluble forms. CD48 is a high-affinity ligand for 2B4 and a low-affinity ligand for CD2. CD48 has also been referred to in the scientific literature as “TCT.1” (Mami-Chouaib et al., J. Exp. Med. 172:1071-1082 (1990)), “B-LAST 1” (Thorley-Lawson et al., Cell 30:415-425 (1982)), and SLAMF2 (Detre et al., Semin. Immunopathol. 32:157-171 (2010)). The interaction between CD48 and 2B4 was shown to cause NK cell activation. CD48 has also been shown to stimulate T-cell activation in vitro, and CD48-knockout mice display an impaired T-cell proliferation response.
Certain lines of evidence suggest a role for CD48 in asthma progression and inflammatory bowel disease (IBD). For example, CD48 was shown to be upregulated in experimental asthma (e.g., ovalbumin- and Aspergillus-induced allergic eosinophilic airway inflammation models). See, e.g., Munitz et al., Am. J. Respir. Crit. Care Med. 175:911-918 (2007). Moreover, CD48 knock-out mice failed to develop inflammatory colitis in the adoptive transfer model of IBD. Furthermore, CD48 antagonism was shown to produce beneficial effects in previously established colitis.
The use of CD48 antagonists for therapeutic purposes are mentioned in, e.g., US 2007/0212353 and WO 97/35614. Nonetheless, there remains a need in the art for novel CD48 modulating agents, including anti-CD48 antibodies, that can be used to treat CD48-mediated diseases and conditions.